From Wikipedia, the free encyclopedia
A peptic ulcer, also known as ulcus pepticum, PUD or peptic ulcer disease,[1] is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful. As many as 80% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach, however only 40% of those cases go to a doctor. Ulcers can also be caused or worsened by drugs such as aspirin and other NSAIDs.
Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign.
Classification
* Stomach (called gastric ulcer)
* Duodenum (called duodenal ulcer)
* Oesophagus (called Oesophageal ulcer)
* Meckel's Diverticulum (called Meckel's Diverticulum ulcer)
Types of peptic ulcers:
* Type I: Ulcer along the lesser curve of stomach
* Type II: Two ulcers present - one gastric, one duodenal
* Type III: Prepyloric ulcer
* Type IV: Proximal gastroesophageal ulcer
* Type V: Anywhere along gastric body, NSAID induced
Signs and symptoms
Symptoms of a peptic ulcer can be
* abdominal pain, classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
* bloating and abdominal fullness;
* waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus);
* nausea, and copious vomiting;
* loss of appetite and weight loss;
* hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
* melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);
* rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.
A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).
In patients over 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).
The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest mostly before the meal—when acid (production stimulated by hunger) is passed into the duodenum. However, this is not a reliable sign in clinical practice.
Complications
* Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening.[2] It occurs when the ulcer erodes one of the blood vessels.
* Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.
* Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas.[3]
* Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.
* Pyloric stenosis
Cause
A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or increased. Gastrin stimulates the production of gastric acid by parietal cells and, in H. pylori colonization responses that increase gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.
Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western world due to increased medical treatment, a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis.
The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort-phenomena independent of the progress in treatment of the disease. The cohort-phenomena is probably explained by improved standards of living which has lowered the incidence of H. pylori infections.[4]
Tobacco smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia. Nicotine contained in cigarettes can increase parasympathetic nerve activity to the gastrointestinal tract by acting on the nicotinic receptors at synapses - increased stimulation to the enterochromaffin-like cells and G cells increases the amount of histamine and gastrin secreted and therefore increases the acidity of the gastric juice. Similarly, glucocorticoids lead to atrophy of all epithelial tissues. However, these factors, along with diet or spices, blood type, and other factors suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.[5]
Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult to heal ulcers.
Stress
Researchers also continue to look at stress as a possible cause, or at least complication, in the development of ulcers. There is debate as to whether psychological stress can influence the development of peptic ulcers. Burns and head trauma, however, can lead to physiologic stress ulcers, which are reported in many patients who are on mechanical ventilation.
An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role.[1] Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.[6]
A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor.[7]
Differential diagnosis of epigastric pain
# Peptic ulcer
# Gastritis
# Stomach cancer
# Gastroesophageal reflux disease
# Pancreatitis
# Hepatic congestion
# Cholecystitis
# Biliary colic
# Inferior myocardial infarction
# Referred pain (pleurisy, pericarditis)
# Superior mesenteric artery syndrome
Treatment
Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even clear organisms, though it should be noted that the warning labels of some bismuth subsalicylate products indicate that the product should not be used by someone with an ulcer.
Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers, which may be a side-effect of the NSAIDs.
When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.
Treatment of H. pylori usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.
Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.
Epidemiology
The lifetime risk for developing a peptic ulcer is approximately 10%.[10]
In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third world countries. Transmission is by food, contaminated groundwater, and through human saliva (such as from kissing or sharing food utensils.)[citation needed]
According to Mayo Clinic, however, there is evidence that the infection can be transmitted by kissing.[citation needed]
A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort, abdominal pain or gastritis.
